Brain derived β-interferon is a potential player in Alzheimer's disease pathogenesis and cognitive impairment.

Background: Recent research has postulated that the activation of cGAS-STING-interferon signalling pathways could be implicated in the pathogenesis of Alzheimer's disease (AD). However, the precise types of interferons and related cytokines, both from the brain and periphery, responsible for cognitive impairment in patients with AD remain unclear.

Methods: A total of 131 participants (78 [59.

Do Caregivers Value the New Antiamyloid Treatments for Alzheimer's Disease More Than Home-Based Care?

Objective: The new antiamyloid medications Lecanemab (Leqembi) and donanemab (Kisunla) are the first disease-modifying treatments for Alzheimer's disease (AD) to receive full FDA approval. However, some commentators question whether the drugs' benefits outweigh their risks, burdens, and costs to patients. This study assessed the perceived value of these medications by asking caregivers of persons with AD to compare them to a widely used intervention in AD management: home-based care.

Tetrahydrofolic acid accelerates amyloid fibrillization, decreases cytotoxic oligomers and suppresses their toxicity.

Soluble cytotoxic oligomers produced during the fibrillation of both α-synuclein (αS) and amyloid-β protein (Aβ) are key pathogenic factors in Parkinson's disease (PD) and Alzheimer's disease (AD). Reducing toxic oligomers by regulating the aggregation process of αS and Aβ is an important strategy for the treatment of PD and AD. Herein, tetrahydrofolic acid (THF) is found to accelerate amyloid fibrillization, decreases cytotoxic oligomers and suppresses their toxicity.

Modeling functional loss in Alzheimer's Disease through cognitive reserve and cognitive state: A panel data longitudinal study.

Cognitive Reserve (CR) refers to the brain's ability, supported by active and modifiable forms of lifestyle compensation, to cope with neural changes due to age or disease, delaying the onset of cognitive deficits. In CR studies, neuropsychological performances and functional autonomy are considered alternative outcomes. While decreased functional independence gains importance in dementia diagnosis and monitoring, cognitive functioning may play a role in staging its severity.

Qualitative and quantitative relationships between comorbid seizures and dementia among hospitalized stroke patients.

This study examines the relationship between comorbid seizures and dementia among stroke patients using the 2017 Nationwide Inpatient Sample (NIS), the largest publicly available inpatient healthcare database in the United States. We analyzed data from 128,341 stroke patients, including those with ischemic and hemorrhagic strokes, to determine the prevalence of seizures and dementia, and the association between these conditions. Our findings reveal that 7.

Olfactory bulb microglia activation mediates neuronal pyroptosis in ozone-exposed mice with olfactory and cognitive dysfunction.

In recent years, there has been a notable increase in the concentration of air pollutants in the troposphere, especially ozone. However, limited research has gone beyond examining histopathological alterations in the olfactory bulb (OB) to explore the effects of ozone exposure on olfactory and cognitive functions. In our study, we exposed nine-month-old C57BL/6 mice to ozone at a concentration of 1.

Multi-target directed ligands inspired natural products as an effective approach for the treatment of complex chronic health disorders.

Complex diseases involve multifaceted etiological components, which limit the effectiveness of conventional targeted therapies. Therefore, standard medicinal treatments often face significant challenges and failures when addressing these disease conditions. Furthermore, the growing interest in multidrug resistance (MDR), the occurrence of adverse drug reactions related to use traditional approaches, and the limited clinical efficacy of single-target drug therapy have increased the demand for innovative drug treatments.

An objective and sensitive electrophysiological marker of word semantic categorization impairment in Alzheimer's disease.

Objective: Combining electroencephalographic (EEG) recording and fast periodic visual stimulation (FPVS) to provide an implicit, objective and sensitive electrophysiological measure of semantic word categorization impairment in Alzheimer's Disease (AD).

Methods: Twenty-five AD patients and 25 matched elderly healthy controls were tested with a validated FPVS-EEG paradigm in which different written words of the same semantic category (cities) appear at a fixed frequency of 4 words per second (4 Hz) for 70 seconds. Words from a different semantic category (animal) appear every 4 stimuli (i.

Time-Frequency functional connectivity alterations in Alzheimer's disease and frontotemporal dementia: An EEG analysis using machine learning.

Objective: Alzheimer's disease (AD) and frontotemporal dementia (FTD) are prevalent neurodegenerative diseases characterized by altered brain functional connectivity (FC), affecting over 100 million people worldwide. This study aims to identify distinct FC patterns as potential biomarkers for differential diagnosis.

Methods: Resting-state EEG data from 36 AD patients, 23 FTD patients, and 29 healthy controls were analyzed using time-frequency and bandpass filtering FC metrics.

Triple-mode sensing platform for acetylcholinesterase activity monitoring and anti-Alzheimer's drug screening based on a highly stable Cu (I) compound.

Acetylcholinesterase (AChE) and AChE inhibitors play critical roles in the early diagnosis and treatment of Alzheimer's disease (AD). Herein, a fluorescence/colorimetry/smartphone triple-mode sensing platform was constructed for both AChE activity monitoring and AChE inhibitor screening by exploring a Cu (I) compound, CuI (SR) (R = CHCHNH), as a fluorescent probe. In comparison of most other fluorescent probes, CuI (SR) presented exceptional stability against pH, temperature, UV irradiation, redox agents, and metal ions, as well as good recyclability due to its unique chemical structure.

Hypothalamic volume is associated with age, sex and cognitive function across lifespan: a comparative analysis of two large population-based cohort studies.

Background: Emerging findings indicate that the hypothalamus, the body's principal homeostatic centre, plays a crucial role in modulating cognition, but comprehensive population-based studies are lacking.

Methods: We used cross-sectional data from the Rhineland Study (N = 5812, 55.2 ± 13.

Memantine/Rosuvastatin Therapy Abrogates Cognitive and Hippocampal Injury in an Experimental Model of Alzheimer's Disease in Rats: Role of TGF-β1/Smad Signaling Pathway and Amyloid-β Clearance.

Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder of complex pathogenesis and multiple interacting signaling pathways where amyloidal-β protein (Aβ) clearance plays a crucial role in cognitive decline. Herein, the current study investigated the possible modulatory effects of memantine/ rosuvastatin therapy on TGF-β1/p-Smad/p21 signaling pathway and their correlation to the blood brain barrier transporters involved in Aβ-clearance and microRNAs as a novel molecular mechanism in AD treatment. AD was induced by a single intracerebroventricular streptozotocin injection (ICV-STZ, 3 mg/kg) in rats and drug therapy was continued for 28 days after AD induction.

Linking metabolic syndrome, cerebral small vessel disease, and cognitive health: insights from a subclinical population study using TriNetX.

Metabolic syndrome (MetS) has been linked to accelerated cognitive decline and Alzheimer's disease and related dementias (ADRDs) via cerebral small vessel disease (CSVD); however, this relation in MetS without overt cardiometabolic disease comorbidities is unknown and may represent a population amenable to preventative strategies. Our study aimed to determine risk profiles for neurocognitive decline and ADRDs in early-stage MetS with evidence of CSVD using the TriNetX electronic health records (EHR) research network. Patients aged 50 to 80 years old meeting MetS criteria were identified utilizing TriNetX data from 76 healthcare organizations.

Brain MRI volumetry and atrophy rating scales as predictors of amyloid status and eligibility for anti-amyloid treatment in a real-world memory clinic setting.

Predicting amyloid status is crucial in light of upcoming disease-modifying therapies and the need to identify treatment-eligible patients with Alzheimer's disease. In our study, we aimed to predict CSF-amyloid status and eligibility for anti-amyloid treatment in a memory clinic by (I) comparing the performance of visual/automated rating scales and MRI volumetric analysis and (II) combining MRI volumetric data with neuropsychological tests and APOE4 status. Two hundred ninety patients underwent a comprehensive assessment.

Opposite Roles of Cholesterol and Lanosterol in Lipid Membrane on Amyloid-Beta 42 Peptide Nucleation and Fibril Formation.

Molecular self-assembly of amyloid-beta peptides to form fibrillar aggregates is a known cause of Alzheimer's disease. Although homogeneous nucleation of amyloid-beta is unfavorable, heterogeneous nucleation of amyloid-beta in cell membranes plays a key role in fibril formation. We observed these opposite roles in the effects of cholesterol and lanosterol, the precursor of cholesterol in the brain, on nucleation.

Association of critically short telomeres with brain and blood markers of ageing and Alzheimer's disease in older adults.

Background: Accumulation of critically short telomeres (CST) is implicated in decreased tissular regenerative capacity and increased susceptibility to degenerative diseases such as Alzheimer's disease (AD). Telomere shortening has also been associated with age-related brain changes. However, it remains unclear whether CST accumulation is directly associated with AD markers or instead amplifies age-related effects, potentially increasing susceptibility of developing AD in cognitively healthy older adults.

pTau pathology in the retina of TAU58 mice: association with ganglion cell degeneration and implications on seeding and propagation of pTau from human brain lysates.

The accumulation of abnormal phosphorylated Tau protein (pTau) in neurons of the brain is a pathological hallmark of Alzheimer's disease (AD). PTau pathology also occurs in the retina of AD cases. Accordingly, questions arise whether retinal pTau can act as a potential seed for inducing cerebral pTau pathology and whether retinal pTau pathology causes degeneration of retinal neurons.

Paradoxical attenuation of early amyloid-induced cognitive impairment and synaptic plasticity in an aged APP/Tau bigenic rat model.

The combination of amyloid beta and tau pathologies leads to tau-mediated neurodegeneration in Alzheimer's disease. However, the relative contributions of amyloid beta and tau peptide accumulation to the manifestation of the pathological phenotype in the early stages, before the overt deposition of plaques and tangles, are still unclear. We investigated the longitudinal pathological effects of combining human-like amyloidosis and tauopathy in a novel transgenic rat model, coded McGill-R-APPxhTau.

Cognitive decline profiles associated with lewy pathology in the context of Alzheimer's disease neuropathologic change.

Background: Alzheimer's disease neuropathologic change (ADNC) and Lewy pathology (LP) often coexist in cognitively impaired individuals. These pathologies' relative distribution and severity may modify these individuals' clinical presentation, cognitive profile, and prognosis. Therefore, we examined the contributions of LP and concomitant ADNC to disease survival and profiles of cognitive decline in preclinical and clinical stages in a large neuropathologically diagnosed group.

A Review of the Knops Blood Group System.

The Knops blood group system is an independent blood group system recognized by International Society of Blood Transfusion (ISBT) in 1992, and latest time consisting of 13 antigens carried on a glycoprotein of 2489 amino acids and called the Complement C3b/C4b Receptor 1 (CR1). Erythrocyte KN antigen was first reported in 1970, and CR1 is a protein coding gene that is a member of the receptors of complement activation (RCA) family and is located in the "cluster RCA" region of chromosome 1. CR1 is an important participant in the erythrocyte immune machinery and plays an major role in inhibiting complement activation, and polymorphisms in its expression have been closely associated with a variety of diseases, including systemic lupus erythematosus (SLE), malaria, Plasmodium falciparum malaria, Alzheimer's disease (AD) and leprosy.

Brain Metabolic Resilience in Alzheimer's Disease: A Predictor of Cognitive Decline and Conversion to Dementia.

Objective: Brain atrophy measured by structural imaging has been used to quantify resilience against neurodegeneration in Alzheimer's disease. Considering glucose hypometabolism is another marker of neurodegeneration, we quantified metabolic resilience (MR) based on Fluorodeoxyglucose positron emission tomography (FDG PET) and investigated its clinical implications.

Methods: We quantified the MR and other resilience metrics, including brain resilience (BR) and cognitive resilience (CR), using partial least squares path modeling from the ADNI database.